Research led by Dr. Anne Mueller at Stanford University School of Medicine demonstrates that successful eradication of Helicobacter may not prevent future aggressive gastric lymphoma since resting B cells are left behind. The paper by Mueller et al., "The role of antigenic drive and tumor-infiltrating accessory cells in the pathogenesis of Helicobacter-induced MALT lymphoma," appears in the September issue of The American Journal of Pathology.
Helicobacter pylori, a spiral bacterium of the stomach, infects more than half of the world’s population. It is now widely accepted that, aside from gastritis and ulcers, H. pylori is also a causative agent of gastric lymphoma, specifically gastric B cell lymphoma of mucosa-associated lymphoid tissue (MALT). While antibiotic treatment eradicates the bacteria and promotes tumor regression, the effects of re-infection on disease are more severe.
To address the effects of re-infection and the role of immune cells in disease progression, Dr. Mueller’s group used a mouse model of Helicobacter-induced MALT lymphoma that employs H. felis to mimic human disease in the mouse. Mice were infected with H. felis and maintained for 18 months before being assigned to one of three treatment groups: 1) no treatment (primarily infected), 2) antibiotic therapy to eradicate bacteria, or 3) antibiotic therapy followed by re-infection.
Audra Cox | EurekAlert!
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